Alzheimer's Disease: Causes, Symptoms and Treatment

Alzheimer's disease (AD) is the most common form of dementia, accounting for 60–70% of all dementia cases worldwide. It is a progressive, neurodegenerative disorder that destroys memory and cognitive function over years to decades — ultimately impairing the ability to carry out the simplest tasks of daily living.

Approximately 50 million people worldwide are living with dementia, and Alzheimer's disease is responsible for the majority. As populations age, this number is projected to reach 152 million by 2050. In China, over 10 million people are currently living with Alzheimer's disease, making it one of the country's most significant public health challenges.

What Causes Alzheimer's Disease?

Alzheimer's disease is characterised at the cellular level by two abnormal protein accumulations:

Amyloid Plaques

The amyloid precursor protein (APP) is cleaved by secretase enzymes. In Alzheimer's disease, abnormal cleavage produces a 42-amino-acid fragment called amyloid-β (Aβ42) that aggregates into oligomers and then forms insoluble plaques that accumulate outside neurons in the brain. These amyloid plaques disrupt synaptic transmission and trigger neuroinflammation.

The amyloid cascade hypothesis proposes that amyloid accumulation is the initiating event, occurring 10–20 years before symptoms appear. This has driven the development of anti-amyloid therapies.

Tau Neurofibrillary Tangles

Tau is a protein that normally stabilises the internal scaffolding (microtubules) that transport nutrients within neurons. In Alzheimer's disease, tau becomes hyperphosphorylated, detaches from microtubules, and aggregates into twisted tangles (neurofibrillary tangles — NFTs) inside neurons. NFTs spread through the brain in a stereotyped pattern (Braak stages), correlating with cognitive decline.

Neuronal Death and Brain Atrophy

The combined effect of plaques, tangles, and neuroinflammation leads to synaptic dysfunction and progressive neuronal death — particularly in the hippocampus (memory) and entorhinal cortex initially, then spreading to the temporal, parietal, and frontal cortices. The brain shrinks — in late-stage Alzheimer's disease, volume loss can be 20–30% compared to a healthy brain.

Risk Factors

Age is the greatest risk factor — risk doubles approximately every 5 years after 65.

Genetics:

• APOE ε4 allele — the most important genetic risk factor for late-onset sporadic AD. One copy increases lifetime risk approximately 3×; two copies increase risk approximately 8–12×. Present in approximately 25% of the population.
• Early-onset familial AD (before 65, rare): autosomal dominant mutations in PSEN1 (presenilin-1), PSEN2, or APP — nearly 100% penetrance, onset in 40s–50s.

Other risk factors: cardiovascular risk factors (hypertension, diabetes, obesity, dyslipidaemia, smoking) — "what is bad for the heart is bad for the brain"; head trauma (particularly repeated or severe); social isolation; hearing loss; low educational attainment (reduced cognitive reserve); depression.

Protective factors: higher education, cognitive engagement, regular aerobic exercise, Mediterranean diet, social connection.

Stages and Symptoms

Alzheimer's disease progresses through recognisable stages, though the rate varies.

Preclinical Stage (10–20 years before symptoms)

Amyloid accumulates silently. No symptoms. Detectable only by PET imaging or CSF biomarkers. This is the target window for disease-modifying interventions.

Mild Cognitive Impairment (MCI) Due to Alzheimer's

The transitional stage between normal cognition and dementia. The individual notices memory difficulties that others can also observe, but daily function remains largely intact.

Symptoms:

• Forgetting recent events, conversations, or appointments
• Difficulty retaining new information
• Mild word-finding difficulty
• Navigational difficulties in new environments

Approximately 10–15% of MCI patients progress to Alzheimer's dementia per year. Not all MCI is due to Alzheimer's disease.

Mild Alzheimer's Dementia

Memory loss now affects daily life. Family members notice significant changes.

• Repeatedly asking the same questions; forgetting recent conversations
• Getting lost in familiar places
• Difficulty managing finances, planning, or complex tasks
• Personality changes — increased anxiety, withdrawal, irritability, apathy
• Word-finding difficulties; circumlocution (talking around words)

Moderate Alzheimer's Dementia

The person requires assistance with daily activities.

• Unable to recall the names of close family members
• Forgetting personal history (address, phone number, where they were born)
• Confusion about time, day, month, year, and season
• Behavioural symptoms: agitation, wandering, suspicion or paranoia, sleep disturbance, aggression
• Difficulty with dressing, hygiene, and toileting
• Hallucinations (less common than in Lewy body dementia but can occur)

Severe Alzheimer's Dementia

Complete dependence on care.

• Loss of verbal communication — only short phrases or single words
• Inability to perform any activities of daily living (eating, dressing, toileting, bathing)
• Bladder and bowel incontinence
• Loss of mobility — ultimately confined to bed
• Highly susceptible to infections (aspiration pneumonia is the most common cause of death)

Diagnosis

Clinical Assessment

Diagnosis is clinical — based on a careful history from both the patient and an informant who knows the patient well, combined with cognitive testing. The neurologist or geriatrician assesses:

• Pattern of cognitive deficits (episodic memory loss is the hallmark)
• Onset, progression, and functional impact
• Medications, medical history, and vascular risk factors
• Depression and other reversible causes of cognitive impairment

Cognitive tests: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Addenbrooke's Cognitive Examination (ACE) — standardised tools to quantify and track cognitive deficits.

Neuropsychological testing — formal, detailed assessment of memory domains, executive function, language, visuospatial skills, and attention to characterise the pattern and severity of impairment.

Brain Imaging

MRI of the brain — the essential structural investigation. In Alzheimer's disease, MRI shows:

• Disproportionate hippocampal and medial temporal lobe atrophy
• Cortical atrophy in temporal and parietal regions
• White matter changes (leukoaraiosis) reflecting vascular burden
• Exclusion of other causes: brain tumour, subdural haematoma, NPH, vascular dementia

Amyloid PET scan — detects amyloid plaques in the brain decades before symptoms. A negative amyloid PET essentially excludes Alzheimer's disease. Used in clinical trials and increasingly in clinical practice for diagnosis confirmation.

FDG-PET — shows hypometabolism in temporal and parietal cortex; useful for distinguishing AD from other dementias.

Biomarker Testing

Cerebrospinal fluid (CSF) biomarkers — obtained by lumbar puncture:

• Low Aβ42 (amyloid being sequestered in plaques)
• High tau and phospho-tau (reflecting neurodegeneration and tangle formation)
• The "Alzheimer's CSF signature" has high diagnostic accuracy

Blood plasma biomarkers — emerging and rapidly advancing:

• Plasma phospho-tau 217 (p-tau217), amyloid ratio — now commercially available; accuracy approaching CSF
• These are transforming the ability to screen and diagnose AD non-invasively

Treatment

Currently Approved Symptomatic Treatments

No treatment currently reverses or halts Alzheimer's disease progression. Symptomatic treatments modestly improve cognitive function and delay functional decline.

Cholinesterase inhibitors — donepezil (Aricept), rivastigmine, galantamine. Block the breakdown of acetylcholine, a neurotransmitter deficient in AD. Provide modest cognitive and functional benefit in mild-to-moderate AD. Donepezil is also licensed for severe AD. Side effects: nausea, diarrhoea, bradycardia.

Memantine — blocks overactivation of NMDA glutamate receptors, which contributes to excitotoxic neuronal death. Licensed for moderate-to-severe AD. Often combined with a cholinesterase inhibitor. Modest benefit; good tolerability.

Disease-Modifying Therapy — Anti-Amyloid Antibodies

A major milestone in Alzheimer's treatment came with the approval of anti-amyloid monoclonal antibodies that remove amyloid plaques from the brain:

Lecanemab (Leqembi) — FDA-approved 2023; reduced clinical decline by 27% in early Alzheimer's disease in the CLARITY AD trial. Given as IV infusion every two weeks. Requires amyloid PET or CSF confirmation before treatment.

Donanemab (Kisunla) — FDA-approved 2024; reduced clinical decline by 35% in early AD patients with low-to-medium tau burden in the TRAILBLAZER-ALZ2 trial. Given monthly; treatment can be discontinued once amyloid is cleared.

Key limitation — ARIA (amyloid-related imaging abnormalities): these antibodies can cause brain swelling and microbleeds (ARIA-E and ARIA-H), requiring MRI monitoring. APOE ε4 homozygotes carry highest risk. Appropriate candidate selection and MRI surveillance are essential.

These therapies are most effective in early-stage disease (MCI or mild AD) — reinforcing the importance of early biomarker-confirmed diagnosis.

Non-Pharmacological Management

• Cognitive stimulation therapy (CST) — structured group-based activities; level 1 evidence for benefit in mild-moderate AD
• Physical exercise — aerobic exercise slows hippocampal atrophy and improves cognitive outcomes in MCI
• Occupational therapy — home adaptations, daily routine structure, carer training
• Behavioural and psychological symptom management: non-pharmacological approaches first; low-dose antipsychotics only for severe agitation/psychosis with clear risk-benefit assessment
• Carer support — education, respite care, and psychological support for family carers, who carry the greatest burden of AD

Dementia and Alzheimer's Care in China

China's cognitive neurology and memory disorder centres offer:

• Comprehensive memory clinic assessment: clinical evaluation, neuropsychological testing, brain MRI, FDG-PET, and CSF biomarker analysis (tau/Aβ42)
• Amyloid PET imaging: available at leading centres for diagnosis confirmation and anti-amyloid therapy evaluation
• Emerging anti-amyloid therapies: access to lecanemab and donanemab through clinical programmes and regulatory approved pathways at top centres
• Multidisciplinary dementia management: neurology, geriatric psychiatry, occupational therapy, speech therapy, and carer counselling integrated into a single care pathway
• Cost: care in China is generally less expensive than UK private treatment, but the hospital prices each case individually — ask us for the written quote before you commit.
• Full English coordination from assessment through diagnosis and treatment planning

Contact a ChinaMedicalTour care navigator to arrange a memory and cognitive assessment, Alzheimer's disease evaluation, or second opinion on dementia diagnosis.

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Medical content based on MSD Manuals and international Alzheimer's disease guidelines. Evidence reviewed 2025.

Frequently Asked Questions

Can overseas neurological patients have their MRI or EEG scans evaluated remotely?

Yes. Foreign neuroimaging scans, EEG recordings, and specialist consult notes can be submitted through pre-consultation coordination for detailed evaluation by Chinese cognitive neurology and movement disorder teams.

What multidisciplinary care is offered for chronic neurological conditions in China?

Tertiary neurology departments provide structured clinical assessments, cognitive battery testing, advanced biomarker diagnostics, individualized pharmacological management, and specialized neurorehabilitation planning.

How are medications and ongoing neurological care managed after returning home?

The treating medical team issues a comprehensive bilingual medical summary and prescription guidance to facilitate safe care continuity with the patient's domestic neurologist.